Figure 1
Figure 1. DOCK2 deficiency does not affect NK cell development and surface expression of activating receptors. (A) Spleen cells and BM cells were stained for NK1.1 and CD3ε, and the number of NK cells (NK1.1+CD3ε– cells) was compared between WT and DOCK2−/− mice. Data are expressed as the mean ± standard deviation (SD) of 3 mice. (B) The expression of CD27, CD11b, and/or DX5 on NK1.1+CD3ε– NK cells in the spleen and BM was compared between WT and DOCK2−/− mice. Data are representative of 2 independent experiments. (C) Fresh or activated NK cells with IL-2 (1000 U/mL) for the indicated times were prepared from WT and DOCK2−/− mice, and the expression levels of NKG2D and Ly49D were compared by staining the cells with relevant antibody followed by Alexa Fluor 488–labeled secondary antibody. As a control, the flow cytometric profile for cells stained with the secondary antibody only is shown. Data are representative of 2 independent experiments.

DOCK2 deficiency does not affect NK cell development and surface expression of activating receptors. (A) Spleen cells and BM cells were stained for NK1.1 and CD3ε, and the number of NK cells (NK1.1+CD3ε cells) was compared between WT and DOCK2−/− mice. Data are expressed as the mean ± standard deviation (SD) of 3 mice. (B) The expression of CD27, CD11b, and/or DX5 on NK1.1+CD3ε NK cells in the spleen and BM was compared between WT and DOCK2−/− mice. Data are representative of 2 independent experiments. (C) Fresh or activated NK cells with IL-2 (1000 U/mL) for the indicated times were prepared from WT and DOCK2−/− mice, and the expression levels of NKG2D and Ly49D were compared by staining the cells with relevant antibody followed by Alexa Fluor 488–labeled secondary antibody. As a control, the flow cytometric profile for cells stained with the secondary antibody only is shown. Data are representative of 2 independent experiments.

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